HIV Exacerbates Atherosclerosis by Altering Macrophage Function

Human immunodeficiency virus (HIV) infection and atherosclerosis affect millions of people worldwide.HIV exerts profound effects on macrophages, which are cells that play a central role in the initiation and progression of atherosclerotic lesions.Accordingly, although the prevalence of subclinical atherosclerotic plaque among people living with HIV (PLHIV) is similar to that observed in the general population, PLHIV experience higher rates of myocardial infarction and other adverse cardiovascular events.In this review, we summarize current knowledge regarding the interplay between HIV and macrophage biology in the context of atherogenesis, and discuss additional pro-atherogenic mechanisms attributable to the virus.In addition, we examine how specific HIV proteins drive macrophage polarization toward pro-inflammatory phenotypes through upregulation of cytokines, surface receptors, and dysregulated lipid uptake.These pathways contribute to, and are amplified by, chronic systemic inflammation, which is a characteristic feature of HIV infection.Furthermore, we consider the impact of HIV-induced alterations of circulating monocytes, which differentiate into macrophages once recruited to developing plaques, thereby linking systemic immune dysregulation to local vascular pathology.